Will Viagra One Day Coat Coronary Stents?

Mouse model findings are suggestive for reduced restenosis

An erectile dysfunction drug may show promise for future drug-eluting stents (DES), according to a series of basic science experiments.

Sildenafil (Viagra) reduced both platelet aggregation and a marker of restenosis, which could give it a potential edge over both bare metal stents and current-generation DES, reported Han-Mo Yang, MD, PhD, of Seoul National University Hospital in South Korea, and colleagues in a poster at the American Heart Association's Basic Cardiovascular Sciences 2017 meeting.

The drug activates protein kinase G (PKG) and was found to reduce neointimal hyperplasia in rat carotid arteries. Furthermore, Yang's group found that sildenafil reduced viability, cell cycle progression, and migration of vascular smooth muscle cells and inhibited their change from a contractile to a synthetic form.

A PKG blocker could reverse sildenafil's inhibition of platelet aggregation (induced by ADP or thrombin), which seemed to confirm that the drug inhibits platelet aggregation via the PKG pathway.

Separately, a mouse experiment also showed that sildenafil facilitated re-endothelialization.

"This study showed that sildenafil inhibits not only platelet aggregation, but also neointimal hyperplasia through the PKG pathway. These findings suggest that sildenafil could be a promising candidate drug of DES for the prevention of restenosis without other complications such as stent thrombosis," the authors concluded.

Sildenafil could potentially also be given orally after stent implantation, Yang suggested in a statement. "If clinical trials show that sildenafil reduces restenosis after stent placement, it could be used in the clinical setting right away because the drug is already used in the real world for other purposes."

That would be a major "if." The drug, originally developed to treat high blood pressure, wound up in the erectile dysfunction market because of a happy side effect.

"Of course, we have to be cautious in extrapolating results from animal studies of vascular injury and healing, but the concept of a targeted molecular effect rather than non-specific anti-proliferative agents is intriguing and needs further study," commented Donald Cutlip, MD, of Boston's Beth Israel Deaconess Medical Center, in an interview. He was not involved in the study.

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